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| || INFLAMMATION IS A COMPONENT OF THE PATHOGENESIS of a number of human diseases. The inflammatory response is initiated by the release of a variety of chemical mediators which induce acute or chronic inflammatory condition depending on the amount and the intensity of the mediator release. Mast cells play a critical role in allergic and inflammatory diseases. Allergies are a sign of an immune system run amok. Certain individuals are predisposed to the production of IgE, which binds to the high affinity receptors on mast cells. Subsequent crosslinking of these receptors by appropriate antigen leads to the explosive release of inflammatory mediators, including histamine, prostaglandins leukotrienes, and certain immunoregulatory cytokines. These mediators alone or in concert can induce vigorous inflammatory reaction which sometimes causes fatal anaphylaxis. The mast cell mediator release is the consequence of a cascade of tyrosine kinase mediated signaling events. The goal of our research is to understand mechanisms involved in the mast cell mediator release which would lead to more rational therapeutic or prophylactic treatment for the management of patients suffering from allergies. |
However, in chronic inflammation conditions several other cell types, such as T-cells, macrophages, epithelial and epidermal cells, along with mast cells, play a role in perpetuation and maintenance of inflammation. We have observed that these cell types contribute to inflammation by activation through a specific signaling pathway. Utilizing this information we are developing novel strategies to prevent and treat inflammatory diseases, such as rheumatoid arthritis, Crohn's disease, interstitial cystitis and skin sunburn.
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